An absence of inertia force in patients with PSF is one of the causes of isolated diastolic dysfunction in patients with CAD. Normal LV apical wall motion is substantial enough to give inertia to late systolic aortic flow.
Recently, the importance of central blood pressure for cardiovascular risk stratification has been emphasized. Accordingly, the differences in peak systolic and bottom diastolic pressures between the ascending aorta and the brachial artery should be clarified. Study subjects consisted of 82 consecutive patients with suspected coronary artery disease who underwent cardiac catheterization, and in whom ascending aortic pressure waveform was obtained using a catheter-tipped micromanometer, and at the same time systolic and diastolic pressures were measured (single measurement) from the right upper arm with a cuff-type sphygmomanometer based on the oscillometric technique. No significant systematic difference (bias) was found between the peak pressure obtained in the ascending aorta and the systolic pressure from the right upper arm (133.6 +/- 25.1 vs 131.8 +/- 21.5 mmHg, not significant). Bland-Altman analysis showed only a small bias of +1.8 mmHg, and the limits of agreement were 25.4 mmHg and -21.8 mmHg. In contrast, the bottom pressure in the ascending aorta was significantly lower compared with the diastolic pressure from the upper arm (68.5 +/- 10.7 vs 73.0 +/- 12.4 mmHg, P < 0.0001). Bland-Altman analysis showed a small but significant bias of -4.5 mmHg, and the limits of agreement were 14.1 mmHg and -23.1 mmHg. The observed biases seemed to remain within practical range. However, random variation in the two measurements was rather large. This is considered to be caused by the random error in the single measurement with the cuff-type sphygmomanometer.
and was admitted there. The day before admission, he was given a non-steroidal anti-inflammatory drug by his referring doctor to reduce his pain. He had been followed-up for atrial fibrillation and hypertension without any medication for 11 years.Physical examination on admission revealed fever elevation (38°C) and atrial fibrillation (heart rate, approximately 86 bpm) in addition to right abdominal tenderness. His blood pressure was 156/93 mmHg. Laboratory examination of blood showed a marked rise in lactate dehydrogenase (LDH: 2,161 IU/l) and slight rises in two transaminases, aspartate aminotransferase (AST: 340 IU/l) and alanine aminotransferase (ALT: 275 IU/l), while alkaline phosphatase (Al-Pase) was not elevated (Table 1). The serum creatinine concentration was normal (1.0 mg/dl). White blood cell counts (10,000/µl), C reactive protein (1.70 mg/dl) and D-D dimer (1.8 µg/ml) were slightly elevated, while eosinophilia (0.0%) was not recognized. Plasma renin activity (2.5 ng/ml/h) was slightly elevated, while plasma aldosterone concentration (67 pg/ml) remained normal. Initial urinalysis with a dipstick showed no hematuria, but proteinuria (2 ) was present. Microscopic examination of urinary sediment showed no casts
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